| Project/Area Number |
04671090
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
AMEMIYA Akira (1993) Hokkaido University, School of Dentistry, Professor, 歯学部, 教授 (80018415)
進藤 正信 (1992) 北海道大学, 歯学部, 助手 (20162802)
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| Co-Investigator(Kenkyū-buntansha) |
IIZUKA Tadashi Hokkaido University, School of Dentistry, Instructor, 歯学部, 助手 (80168062)
FUJINAGA Kei Sapporo Medical University, Cancer Research Institute, Professor, 附属がん研究所, 教授 (10045338)
KOHGO Takao Hokkaido University, School of Dentistry, Assistant Professor, 歯学部, 助教授 (80001949)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1992: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | HPV / Oral Squamous Cell Carcinoma / Normal Oral Epithelium / Lymph Node Metastasis / PCR / SSCP / p53 / PCNA / 口腔扁平上皮癌 / ヒトパピローマウイルス(HPV) / 癌遺伝子 |
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| Research Abstract |
1) We investigated the prevalence rate of HPV DNAs in normal mucosa in the oral region. The nested PCR method was utilized to detect target DNA sequences using the HPV E6/E7 consensus primer pair. Of 56 patients examined, HPV 6 and HPV 16 DNA sequences were detected in a 46-year-old male and a 35-year-old female, respectively. These results suggest that HPVs are uncommon in normal oral epithelium.
2) We examined 79 cases of oral squamous cell carcinoma (SCC) utilizing PCR and dot blot hybridization to detect HPV DNA.HPV-16 DNA was detected in 23 cases of oral SCC and both HPV-16 and HPV-18 DNA were detected in one case of tongue SCC.HPV-16DNA was identified predominantly in cancer cells which showed morphological resemblance to basal cells and reduced its hybridized signal in keratinized cells by in situ hybridization. Immunohistochemical detection of PCNA revealed that its close relationship to HPV-16 DNA identified cancer cells. These results suggest that HPV-16 DNA sequences might ha
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ve the ability to maintain the proliferative state of epithelial cells, and it may contribute to the production of malignant phenotype.
3) Twenty cases of oral SCC with cervical lymph node metastasis were investigated for the involvement of HPV DNAs utilizing PCR and dot blot hybridization. HPV DNAs were detected in five cases. Four primary lesions contained HPV-16 DNA,and one contained both HPV-16 and HPV-18 DNAs out of 20 cases examined. The same types of HPV DNAs as those found in primary lesions were detected in metastatic lymph nodes including the one with HPV-16 and HPV-18.
4) We examined 16 primary oral SCCs for detection of p53 mutations and HPV DNAs. Exon 5 through 8 of the p53 gene were examined using PCR-SSCP method. p53 mutations were observed in 4 cases (25.0%). HPV-DNA detection was performed using PCR with consensus primers. HPV-16 DNA was detected in 8 cases (50.0%). p53 mutation and HPV DNA were simultaneously detected in two intraosseus SCCs of the mandible.
These finsings suggest that 1) genesis of oral SCC with HPV infection is different from HPV-negative SCCs ; 2) mutation of the p53 gene in HPV-positive cancer may be secondary event during tumor progression ; 3) inactivation of p53 function by mutation and/or HPV infection are one of important genetic events in the development of SCC in the oral cavity ; 4)other oncogenes or tumor suppressor genes may be crucial to prescribe poor prognosis in oral SCC. Less
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